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AR mediate the actions of testosterone (T) and a more biologically active form, 5α-dihydrotestosterone (DHT), which are the male sex hormones required for development of the male reproductive system and secondary sexual characteristics. This receptor, located on the X chromosome, is expressed in a diverse range of tissues, because they have significant biological actions in many systems <ref name="Bench to Bedside">PMID: 27057074</ref>. There are other androgens that bind with much less potency than T and DHT such as androstenedione, androstenediol, and dehydroepiandrosterone (DHEA) <ref>PMID: 36376977 </ref>.

DBD is a cysteine-rich region that is the most highly conserved one of the steroid hormone nuclear receptor family <ref>PMID: 24909511 </ref>, but it has been shown that binding of selective androgen response elements (AREs) allow the specific activation functions of the AR. They facilitate direct DNA binding of the AR to the promoter and enhancer regions of AR-regulated genes, thereby allowing the activation functions of the N-terminal and ligand binding domains to stimulate or repress the transcription of these genes <ref name="Bench to Bedside" />.

-The ligand-dependent AF-2: is located in the ligand binding domain <ref name="Bench to Bedside" />. <scene name='85/857155/H12_androgen_receptor/1'>H12</scene> forms the core of this region and acts as a lid to close the LBP upon agonist binding <ref>PMID: 24909511 </ref>. It is important for forming the coregulator bindings site as well as mediating direct interactions between the N-terminal and ligand binding domains. Key differences in the contribution of specific conserved residues in the AF-2 core domain between the AR and other steroid hormone nuclear receptors have been identified, it would explain the differences in the structure and the function, as well as the coregulatory proteins they interact with <ref name="Bench to Bedside" />.

This leads to the initiation of transcription, cell proliferation and survival, and negative feedback to inactivate AR transcription <ref name="Bench to Bedside" />.

It has been shown that the androgen/AR complex activates 2nd messenger pathways including ERK, Akt and MAPK and that it interferes with several key proteins including forkhead box protein A1 (FOXA1), PI3K and receptor tyrosine kinases, including ERBB2 and ERBB3. These effects occur within seconds to minutes of androgen treatment <ref name="Bench to Bedside" /><ref>PMID: 28301631</ref>.

There are studies that suggest that some of the non-DNA binding-dependent actions of androgens are mediated via the activation of membrane-bound protein receptors. For instance, the iron-regulated transporter-like protein 9 (ZIP9) mediates the androgen-induced apoptosis of ovarian follicle cells, prostate and breast cancer cells <ref name="Bench to Bedside" />.

Although the physiological significance of the non-DNA binding-dependent actions of the AR is not yet fully defined, it has been proposed that they may oppose the DNA binding-dependent actions and serve as a brake to fine-tune androgen action in target tissues <ref name="Bench to Bedside" />.

It has been demonstrated that AR has the potential to be activated through ligand-independent mechanisms by a number of different growth factors, via phosphorylation of the AR or following interaction with co-activators <ref name="Bench to Bedside" />.

AR is expressed in many tissues, so androgens have been documented to have significant biological actions in bone, muscle, prostate, ovaries, endometrium, bladder, skin, cardiovascular, immune, neural and hematopoietic systems <ref name="Bench to Bedside" /><ref>PMID: 29481861</ref>.